Basal keratinocyte tetrasomy in low-grade squamous intra-epithelial lesions of the cervix is restricted to high and intermediate risk HPV infection but is not type-specific

A Giannoudis, MF Evans, SA Southern, Charles Simon Herrington

Research output: Contribution to journalArticlepeer-review

28 Citations (Scopus)

Abstract

Human papillomavirus (HPV) infection appears to be an early event in cervical carcinogenesis with additional abnormality being required for biological transformation. We have analysed 179 low-grade cervical squamous intra-epithelial lesions (SILs) and 15 normal cervices for the presence of HPV using both in situ hybridization and polymerase chain reaction (PCR). PCR was performed with GP5+/GP6+ primers followed by hybridization using probes for low (HPV 6, 11, 40, 42, 43, 44), intermediate (HPV 31,33, 35, 39, 51, 52, 58, 59, 66 and 68) and high-risk HPVs (HPV 16, 18, 45 and 56). Interphase cytogenetic analysis using pericentromeric probes for chromosomes 1, 3, 4, 6, 10, 1 1, 17, 18 and X was also performed to identify numerical chromosomal abnormalities. Tetrasomy of ail nine chromosomes was identified within basal keratinocytes, was restricted to epithelia infected with high risk (17 of 46) or intermediate risk (23 of 83) HPVs but was not HPV type-specific. Tetrasomy was not identified in any of the epithelia infected with low risk HPVs (n = 62). These numbers include multiple infection. These findings indicate that the induction of tetrasomy is a property restricted to high and intermediate-risk HPV types but that it is not type-specific. The factors governing which lesions will develop this abnormality are as yet unclear. (C) 2000 Cancer Research Campaign.

Original languageEnglish
Pages (from-to)424-428
Number of pages5
JournalBritish Journal of Cancer
Volume82
Issue number2
DOIs
Publication statusPublished - Jan 2000

Keywords

  • cervix
  • human papillomavirus
  • keratinocyte
  • chromosome
  • HUMAN PAPILLOMAVIRUS TYPE-16
  • PROMOTER USAGE
  • NEOPLASIA
  • DIFFERENTIATION
  • AMPLIFICATION
  • CYTOGENETICS
  • EXPRESSION
  • CARCINOMA
  • INDUCTION
  • GENOTYPES

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